Alterations of metabolic and hemodynamic parameters during whole body hyperthermia on the ICU

Introduction

Whole body hyperthermia (WBH) has received renewed interest for the treatment of metastatic cancer [1]. Using a radiant heat device for induction and maintenance of WBH has been shown to have little toxicity [2]. However, the acute cardiovascular and metabolic changes during the treatment are pronounced [3].

Methods

After informed consent, in 12 ASA II patients with metastatic malignant disease who were eligible for WBH hemodynamic, metabolic parameters, lactate and catecholamine plasma concentrations were studied over a 24 h period. The heating device was a RHS-7500, Enthermics Medical Systems, Inc., Menomonee Falls, WI, USA. Target temperature was 41.8°C, time at target was 60 min. Anaesthesia was total intravenous anaesthesia by TCI using propofol (4-6 µg/kg/min). Patients were intubated and mechanically ventilated with an FiO₂, of 0.4 after induction with sufentanil (0.3-0.4 µg/kg), propofol and rocuronium (0.8 mg/kg). Measurements were taken at baseline, during heating, at plateau, after reaching baseline temperature and at 24 h post plateau. Hemodynamic data consisted of HR, MAP, CVP, PAP, PCWP, CI, SVR. Metabolic data were obtained by indirect calorimetry (Puritan Bennett 7250 Metabolic Monitor, Puritan-Bennett-Hoyer GmbH, Bremen, Germany) and consisted of VO₂, VCO₂, RQ and energy expenditure (EE).

Results

During heating and plateau at 41.8°C an increase of cardiac index from baseline of up to 140% could be observed, which was due to a decrease of SVR and MAP. HR increased to 138 ± 27 bpm. CVP, PCWP and PAP did not change significantly. VO₂ increased from 176 ± 23 ml/min to 372 ± 62 ml/min, EE from 1232 ± 51 kcal/day to 2214 ± 62 kcal/day and VCO₂ from 156 ± 21 ml/min to 303 ± 33 ml/min. The values remained elevated after the patients had returned to baseline core temperature. Lactate plasma concentrations did not change significantly. Plasma levels of noradrenaline changed from 156 ± 140 µg/l after induction of anaesthesia to 699 ± 302 µg/l during plateau, adrenaline levels increased slightly from 40 ± 48 µg/l to 67 ± 64 µg/l. Arrhythmia, myocardial ischemia or left ventricular failure were not observed. Pulmonary and renal function remained undisturbed.

Discussion

During WBH, the changes of cardiovascular and metabolic parameters are severe but in our patients did not compromise cardiac, pulmonary or renal function. However, great care must be taken to exclude patients with cardiorespiratory pathology. Elevation of the body temperature to 41.8°C was accompanied by a fourfold rise in plasma noradrenaline, reflecting high sympathetic nerve activity. Plasma adrenaline remained almost unchanged during plateau. The pronounced heat-induced hyper-metabolism and the endocrine response to heating were not abolished by general anaesthesia and were present throughout the observation period. Lactate levels did not rise significantly, suggesting that metabolism remained aerobic. To compensate for the massive loss of peripheral vasomotor tone, aggressive fluid replacement guided by invasive monitoring is recommended for management of patients undergoing WBH. Further studies will determine what type of anaesthetic management should be preferred.